A number of experimental procedures is now known to stimulate an increase in spontaneous NaCl intake in rats. The various conditions under which a salt appetite appears suggests that the mechanisms involved in its genesis are complicated and probably multiple. A working hypothesis, based on studies carried out in this and other laboratories is that blood level of mineralocorticoid hormones, especially aldosterone, controls the appetite for NaCl. Hence, experimental procedures affecting adrenal secretion of mineralocorticoids and their concentration in blood may be expected to affect salt appetite in rats. The mechanism by which mineralocorticoids exert control over sodium intake may be associated with changes in concentration of salivary sodium, potassium or the ratio of the two. Thus, alterations in the composition of the medium bathing taste receptors may alter preference or detection threshold for NaCl. The latter may be translated into specific behavioral changes by electrical impulses from taste receptors to hypothalamic and other brain areas mediating salt appetite. NaCl appetite may also be mediated by direct interaction of mineralocorticoid (MC) (and glucocorticoid, GC) hormones with Type I (MC specific) and Type II (GC specific) receptors in brain, salivary glands and kidney. Experiments are designed to measure the number and affinity, as well as the up- and down- regulation of these receptors for their ligands and to correlate these measurements with the appetite for NaCl induced by a variety of experimental techniques, including adrenalectomy, treatment with hydrochlorothiazide and captopril and spontaneously-induced hypertension. Changes in number and affinity of these receptors following administration of graded doses of MC hormone to each of these groups will also be measured and compared with their intake of NaCl solution under similar circumstances. Experimental procedures affecting function in areas of the brain in which MC hormones localize will also be used to determine their effect on salt appetite in rats.